Living tissues possess known bioelectrical properties. Potential differences can be observed in living tissues during normal function. For example, a potential difference (the “resting potential”) of approximately −70 milliVolts exists between the inside and the outside of normal cell membranes. In certain specialized cell types, such as those found in the cardiac tissues, the potential difference across the cellular membrane slowly changes with time, eventually reaching a threshold that triggers rapid membrane depolarization.
The electrical characteristics of tissue are also observed in damaged tissues. The implantation of one or more pacing leads with electrodes for a cardiac rhythm management (CRM) system, such as a pacemaker or resynchronization device, involves trauma to the tissues, causing damage. This trauma may be caused at least in part by the simple placement of a pacing lead in heart tissue during normal CRM system implantation. More specifically, during implantation of a pacing lead for a CRM system, an elevation of the ST-segment of an electrocardiogram (ECG) is commonly observed, known as a repolarization abnormality, once contact between the electrode disposed at the end of the lead and the cardiac tissue is made. Also known as “current of injury,” this repolarization abnormality may persist anywhere from only a few minutes to occasionally hours. The repolarization abnormality is therefore typically absent from prolonged (“chronic”) lead performance.
It is known that an electrical stimulation applied to tissues may bring about desired effects. One obvious example is the use of electrical stimulation to bring about the clearly observable contraction of the heart muscle. Another much more subtle example is the use of electrical stimulation to alter the wound healing process.
It is also known in the art that electrical stimulation increases the healing rate in both animals and humans. Furthermore, evidence suggests that electrical stimulation can increase scar tissue development, encapsulation, and/or collagen deposition. Scar tissue development, encapsulation, and collagen deposition, generically referred to herein as a foreign body tissue response, are natural responses by a tissue to an implanted foreign object. For example, as shown in FIG. 1, a generic foreign object 100 implanted into a body tissue develops a fibrous encapsulation 110 around the foreign object's surface.
The research still further suggests that this foreign body tissue response, or healing enhancement, take place preferentially at the cathode. This may be significant because the cathode is the preferred polarity used for chronic cardiac stimulation in CRM devices such as pacemakers and resynchronization devices. It is believed that such a foreign body tissue response around a cathodic electrode alters voltage stimulation thresholds, or the voltage potential necessary to incite cardiac contraction. Specifically, as the natural tissue encapsulation surrounding an implanted electrode grows more extensive over time, the voltage needed to stimulate the tissue also increases. These studies show increased encapsulation with pacing and suggest undesirable alterations in electrical performance as a result of pacing.
The increased voltage stimulation thresholds associated with a foreign body tissue response are deleterious to a CRM system for several reasons. First, the higher voltages necessary for stimulation require greater current from the system's battery, thereby decreasing battery life for the system. Higher voltage stimulation may also impair the ability of the CRM system to rapidly sense the effectiveness of an electrical pulse communicated to stimulate the tissue. Further, higher voltage stimulation may result in electrochemical reactions at the electrode/tissue interface, the by-products of which possibly being toxic to the tissue.
FIG. 2 illustrates how typical voltage stimulation thresholds for two cathodic electrodes implanted in a heart tissue change over time. The voltage stimulation threshold is the voltage necessary to cause a desired effect on a tissue. For example, with cardiac tissue, the voltage stimulation threshold may be the voltage necessary to cause the cardiac tissue to contract. The x-axis in FIG. 2 represents time, in weeks, and the y-axis represents the voltage stimulation threshold necessary for stimulation of a cardiac tissue.
The first solid line A illustrates the voltage stimulation thresholds necessary for a typical electrode implanted into a cardiac tissue. A typical voltage stimulation threshold necessary to stimulate the tissue upon implantation is approximately 0.3 volts. As shown by line A, the stimulation threshold rises over the first two weeks of electrode implantation, peaking at approximately 1 to 2 volts, or possibly more. The stimulation threshold then plateaus and reaches a chronic threshold of approximately 1 volt after approximately four weeks of implantation.
The second dashed line B of FIG. 2 represents the voltage stimulation thresholds necessary for an implanted electrode that includes drug-eluting properties to counteract the foreign body tissue response after introduction of the electrode. One example of such a drug-eluting electrode is disclosed in U.S. Pat. No. 4,819,661 to Heil, Jr. et al., herein incorporated by reference in its entirety. One such drug that may be used to counteract the foreign body tissue response is a steroid. The voltage stimulation threshold for the drug-eluting electrode starts initially at the same 0.3 volts upon implantation, and the threshold peaks at approximately two weeks at approximately 0.8 volts. Finally, the stimulation threshold may reach a chronic level of approximately 0.7–0.8 volts at about four weeks. Therefore, although the drug-eluting electrode exhibits lower peak and chronic stimulation thresholds than a non drug-eluting electrode, there still exists a need to provide an electrode that exhibits still lower peak and chronic thresholds, as well as a lower threshold level at implantation.
It is believed that the mere act of pacing a heart from an implanted CRM system influences the type and rate of healing that occurs around the implanted electrode, causing a greater foreign body tissue response and encapsulation than if pacing was not performed. More specifically, the influence of cathodic pacing on promoting tissue encapsulation is believed to prevent optimized electrode performance. Optimized electrode performance may be achieved only when the tissue-promoting effects of pacing stimuli are minimized or eliminated.
It is therefore desirable to develop a system and method to decrease the foreign body tissue response to implanted electrodes and thereby decrease the voltage thresholds necessary to incite contraction.